Xanthomonas campestris pv. vesicatoria (Xcv) is the causal agent of bacterial spot disease on pepper and tomato. A type III secretion system, which translocates a minimum of 20 effectors into the host cell cytoplasm, is essential for the bacteria's pathogenicity. Some effectors contribute to the pathogen's virulence in suceptible plants. In resistant plants one or several effectors are recognized by the plant immune system, which results mostly in induction of the hypersensitive response (HR). One effector is XopC, which exhibits a predicted haloacid dehalogenase (HAD)-like hydrolase domain and localised to the plant cell cytoplasm and the nucleus. The absence of xopC in the genome of Xcv led to an accelerated HR in resistant pepper plants, if the plants were additionally stressed by exogenous application of salicylic acid (SA). This was complemented by xopC, but not by a xopC derivative carrying a mutation in the predicted HAD-like hydrolase sequence. Yeast-2-hybrid studies revealed a XopC interactor, which also interacted with XopC in planta. The interactor is a functional cytosolic O-acetylserine (thiol)lyases (OAS-TL). In vitro OAS-TL activity was enhanced by adding XopC. Virus-induced gene silencing of OAS-TL in planta abolished the acceleration of the HR formation induced by the absence of xopC in Xcv in resistant pepper plants dependent on SA. These data suggest, that the induction of the HR in resistant pepper plants is SA-stress dependently delayed by XopC, which is reliant on a HAD-like hydrolase domain in XopC. This delay is mediated by the XopC plant interaction partner OAS-TL.